ASD in mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB31117 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3144300_1.fastq.gz | Fastqsanger.gz | |||
| ERR3144300_2.fastq.gz | Fastqsanger.gz | |||
| ERR3144310_1.fastq.gz | Fastqsanger.gz | |||
| ERR3144310_2.fastq.gz | Fastqsanger.gz | |||
| ERR3144320_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 234 |
Similar Datasets
Project description:Gut Microbiota from Human Autism Spectrum Disorder Induces Behavioral Deficits in Mice
| PRJNA432094 | ENA
Project description:Autism spectrum disorder (ASD) manifests as alterations in complex human behaviors including social communication and stereotypies. In addition to genetic risks, the gut microbiome differs between typically-developing (TD) and ASD individuals, though it remains unclear whether the microbiome contributes to symptoms. We transplanted gut microbiota from human donors with ASD and TD controls into germ-free mice, and reveal that colonization with ASD microbiota was sufficient to induce hallmark autistic behaviors. The brains of mice colonized with ASD microbiota display alternative splicing of ASD-relevant genes. Microbiome and metabolome profiles of mice harboring human microbiota predict that specific bacterial taxa and their metabolites modulate ASD behaviors. Indeed, treatment of an ASD mouse model with candidate microbial metabolites improves behavioral abnormalities and affects neuronal excitability in the brain. We propose that the gut microbiome modulates behaviors in mice via production of neuroactive metabolites, suggesting that gut-brain connections contribute to the pathophysiology of ASD.
2019-07-04 | MTBLS726 | MetaboLights
Project description:Intestinal microorganisms impact on health maintaining gut homeostasis and shaping the host immunity, while gut dysbiosis associates with many conditions including autism, a complex neurodevelopmental disorder with multifactorial aetiology. In autism, gut dysbiosis correlates with symptom severity and is characterized by a reduced bacterial variability and a diminished beneficial commensal relationship. Microbiota can influence the expression of host microRNAs that, in turn, regulate the growth of intestinal bacteria by means of bidirectional host-gut micro-biota cross-talk. We investigated possible interactions among intestinal microbes and between them and host transcriptional modulators in autism. To this purpose, we analysed, by “omics” technologies, faecal microbiome, mycobiome and small non-coding-RNAs (particularly miRNAs and piRNAs) of children with autism and neurotypical development. Patients displayed gut dysbiosis, related to a reduction of healthy gut micro- and mycobiota, and up-regulated tran-scriptional modulators. The targets of dysregulated non-coding-RNAs are involved in intestinal permeability, inflammation and autism. Furthermore, microbial families, underrepresented in patients, participate to the production of human essential metabolites negatively influencing the health condition. Here, we propose a novel approach to analyse faeces as a whole and, for the first time, we detected miRNAs and piRNAs in faecal samples of patients with autism.
2022-03-12 | GSE198199 | GEO
Project description:RNAseq analysis of shRNA-mediated knockdown of chromatin modifiers associated with Autism Spectrum Disorder
2022-07-18 | GSE193663 | GEO
Project description:DNA from ectodermal cells of individuals with an Autism Spectrum Disorder born to mothers aged 35 and older was analzyed for discovery of differentially methylated regions and comethylation modules associated with ASD
2014-05-05 | GSE50759 | GEO
Project description:DNA from ectodermal cells of individuals with an Autism Spectrum Disorder born to mothers aged 35 and older was analzyed for discovery of differentially methylated regions and comethylation modules associated with ASD DNA from 48 individuals with ASD and DNA from 48 typically developing controls (all born to mothers older than 35) was isolated, bisulphite converte, and hybridized to the Illumina 450K array.
2014-05-05 | E-GEOD-50759 | biostudies-arrayexpress
Project description:Changes in gut microbiota have been implicated in patients' pathophysiology and cognitive capabilities suffering from autism spectrum disorder. Yet, factors that mediate this interaction remain not fully understood. In this study, we analyzed stool samples from autistic pediatric patients and healthy individuals. Using multi-omics platforms, we characterized microbiota diversities, proteins, and possible altered metabolic pathways.
2021-07-14 | MSV000087817 | MassIVE
Project description:Austism spectrum disorder (ASD) is a heterogeneous behavioral disease most commonly characterized by severe impairment of social engagement and the presence of repetitive activities. The molecular etiology of ASD is still largely unknown despite a strong genetic component. Part of the difficulty in turning genetics into disease mechanisms and potentially new therapeutics is the sheer number and diversity of the genes that have been associated with ASD and ASD symptoms. The goal of this work is to use shRNA-generated models of genetic defects proposed as causative for ASD to identify the common pathways that might explain how they produce a common clinical outcome. Transcript levels of Mecp2, Mef2a, Mef2d, Fmr1, Nlgn1, Nlgn3, Pten, and Shank3 were knocked-down in mouse primary neuron cultures using shRNA/lentivirus constructs. Whole genome expression analysis was conducted for each of the knock-down cultures as well as a mock-transduced culture and a culture exposed to a lentivirus expressing luciferase. Gene set enrichment and a causal reasoning engine were employed to indentify pathway level perturbations generated by the transcript knock-down. Quantitation of the shRNA targets confirmed the successful knock-down at the transcript and protein levels of at least 75% for each of the genes. After subtracting out potential artifacts caused by transfection and viral infection, gene set enrichment and causal reasoning engine analysis showed that a significant number of gene expression changes mapped to pathways associated with neurogenesis, long-term potentiation, and synaptic activity. This work demonstrates that despite the complex genetic nature of ASD, there are common molecular mechanisms that connect many of the best established autism candidate genes. By identifying the key regulatory checkpoints in the interlinking transcriptional networks underlying autism, we are better able to discover the ideal points of intervention that provide the broadest efficacy across the diverse population of autism patients. n=4 per group. Luciferase shRNA used as control group for shRNA to various gene targets.
2013-05-23 | E-GEOD-47150 | biostudies-arrayexpress
Project description:Fragile X Syndrome is an inherited X-linked disorder associated with intellectual disabilities that begin in childhood and last a lifetime. The symptoms overlap with autism spectrum disorder, and the syndrome predominantly affects males. Consequently, FXS research tends to favor analysis of social behaviors in males, leaving a gap in our understanding of other behavioral traits, especially in females. Here we used a mouse model of FXS to analyze developmental, behavioral, neurochemical, and transcriptomic profiles in males and females. Our behavioral assays demonstrated locomotor hyperactivity, motor impulsivity, increased “approach” behavior in an approach-avoidance assay, and deficits in nest building behavior. Analysis of brain neurotransmitter content revealed deficits in striatal GABA, glutamate, and serotonin content. RNA sequencing of the ventral striatum unveiled expression changes associated with neurotransmission as well as motivation and substance use pathways. Sex differences were identified in nest building behavior, striatal neurotransmitter content, and ventral striatal gene expression. In summary, our study identified sex differences in specific behavioral, neurotransmitter, and gene expression phenotypes and gene set enrichment analysis identified significant enrichment of pathways associated with motivation and drug reward.
2024-08-26 | GSE275170 | GEO